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PubMed2005

Relationship between serum adiponectin level and lipid composition in each lipoprotein fraction in adolescent children.

The association of lipid composition in each lipoprotein fraction with adiponectin level in relation to body fatness was investigated. The subjects were 283 children (144 boys and 139 girls) aged 11.6 years (S.D. 1.5). Cholesterol (C) and triglyceride (TG) levels in each lipoprotein fraction were measured by a combination of agarose gel electrophoresis and differential staining. Adiponectin level was not significantly different between girls and boys. In simple regression analyses, an association of adiponectin level with lipoprotein lipid profile was shown only in girls, and not in boys at all. In girls, very low-density lipoprotein (VLDL)-C, low-density lipoprotein (LDL)-C, VLDL-TG and LDL-TG were negatively correlated with adiponectin level, and high-density lipoprotein (HDL)-C and HDL-C/TG ratio were positively correlated. Multiple regression analyses including adiponectin level and body mass index (BMI) as predictors for the lipoprotein lipid profile demonstrated that adiponectin level was a significant independent predictor of VLDL-TG, LDL-C, LDL-TG, HDL-C and HDL-C/TG ratio. In conclusion, adiponectin level correlates with lipoprotein lipid profile independent of body fatness in adolescent girls.

Adiponectin↗
PubMed2005

Inverse association between adiponectin and C-reactive protein in substantially healthy Japanese men.

OBJECTIVE: An inverse association between adiponectin and C-reactive protein (CRP) has been shown in certain pathological states including obesity, diabetes, and coronary artery disease, which themselves might have confounded this association. This study investigated the association between adiponectin and CRP among substantially healthy subjects. METHODS AND RESULTS: A population of 2347 middle-aged Japanese men with no medical history of cardiovascular disease, cancer, diabetes, hypertension, or hyperlipidemia was evaluated. Those with some metabolic syndrome components from serological and anthropometric tests were excluded, leaving 714 men for analysis. Serum adiponectin and CRP were significantly correlated (r = -0.21, P < 0.001). After categorization into quartiles from the lowest to the highest adiponectin concentration (Q1 to Q4), the CRP level was found to be significantly higher in Q1 than in Q2, Q3 and Q4 (0.41 mg/L versus 0.30, 0.25 and 0.24 mg/L, P = 0.043, P < 0.001 and P < 0.001, respectively). These associations remained significant even after adjustment for covariates. Moreover, multiple linear regression analysis revealed that adiponectin contributed more strongly to CRP than other factors, including the index of insulin resistance. CONCLUSIONS: An inverse and strong association between adiponectin and CRP in substantially healthy subjects implies that decreased serum adiponectin might be fundamentally associated with the early stage of low-grade inflammation.

Adiponectin↗
PubMed2006

Low plasma adiponectin exacerbates the risk of premature coronary artery disease in familial hypercholesterolemia.

Familial hypercholesterolemia (FH) is characterized by increased risk for premature coronary artery disease (CAD). This risk is exacerbated in the presence of abdominal obesity and insulin resistance. Low adiponectin is part of the clustering of metabolic abnormalities associated with abdominal obesity and insulin resistance. The present study, therefore, aims to examine the relationship between plasma adiponectin and age at CAD diagnosis in FH patients. Plasma adiponectin was measured by ELISA in 568 non-diabetic FH individuals of French-Canadian origin. CAD was defined according to strict clinical criteria. Prior to analyses, patients were grouped according to age and gender-specific tertiles of plasma adiponectin levels. Multivariate Cox proportional hazards regression was used to estimate the association between plasma adiponectin levels and age at diagnosis of CAD. Overall, FH patients in the lowest tertile of plasma adiponectin exhibited CAD at a significantly younger age (hazard ratio=1.73, confidence interval 95%: [1.19-2.53]; p=0.004). These results suggest that low plasma adiponectin is associated with an increased risk of premature CAD over and above the already exaggerated risk seen in FH patients.

Adiponectin↗
PubMed2005

c-Jun N-terminal kinase is involved in the suppression of adiponectin expression by TNF-alpha in 3T3-L1 adipocytes.

Adiponectin, one of adipokines that is secreted from adipocytes, plays an important role in the regulation of glucose and lipid metabolism. Paradoxically, serum concentrations of adiponectin are decreased in obese and type 2 diabetic patients, although it is produced in adipose tissue. On the other hand, plasma TNF-alpha levels are increased in such subjects. In the present study, the mechanism by which adiponectin is regulated by TNF-alpha was investigated. The decreased adiponectin mRNA levels by TNF-alpha were partially recovered by treatment with a c-Jun N-terminal kinase (JNK) inhibitor or the PPAR-gamma agonist rosiglitazone in 3T3-L1 adipocytes. Interestingly, however, cotreatment with the JNK inhibitor and rosiglitazone led to a recovery of TNF-alpha-mediated adiponectin suppression to the control level. The JNK inhibitor regulated the expression of adiponectin by the increase of PPAR-gamma DNA binding activity and the recovery of its mRNA expression while rosiglitazone acted via a PPAR-gamma independent pathway which remains to be elucidated. These findings suggest that the JNK signaling pathway, activated by TNF-alpha, is involved in the regulation of adiponectin expression.

3T3-L1 Cells↗
PubMed2005

Adiponectin inhibits the binding of low-density lipoprotein to biglycan, a vascular proteoglycan.

The aim of this study was to test the possibility that adiponectin has an antiatherogenic effect through the inhibition of LDL binding to proteoglycans, an initial event in atherogenesis. Both full-length and globular adiponectin inhibited LDL binding in a dose-dependent manner. Both types of adiponectin bound to biglycan in a dose-dependent manner. Immunoprecipitation and immunoblotting analysis showed interaction of full-length adiponectin with LDL. Pretreatment of biglycan with globular adiponectin prior to LDL addition diminished the inhibitory effect, while pretreatment with full-length adiponectin retained the effect. This is a new antiatherogenic property that appears independent of the receptor-mediated hormonal action of adiponectin.

Adiponectin↗
PubMed2006

Oncostatin M decreases adiponectin expression and induces dedifferentiation of adipocytes by JAK3- and MEK-dependent pathways.

Adiponectin, an adipokine secreted from adipocytes, plays a crucial role in the regulation of glucose and lipid metabolism. In the present study, we examine the role of the IL-6 family of cytokines in the expression of adiponectin in human adipocytes derived from human adipose tissue-derived stromal cells. Oncostatin M (OSM), but not IL-6, attenuated the expression level of adiponectin dose- and time-dependently, and the inhibitory effect of OSM on adiponectin expression was as potent as that of TNF-alpha. The OSM-induced down-regulation of adiponectin expression was correlated with the down-regulation of PPARgamma2 and lipoprotein lipase, markers for adipogenic differentiation, and depletion of intracellular lipid droplets, suggesting dedifferentiation of adipocytes in response to OSM. OSM induced phosphorylation of STAT1, and treatment of adipocytes with JAK3 inhibitor WHI-P131 or MEK inhibitor U0126, but not with JAK2 inhibitor AG490, prevented the activation of STAT1. Furthermore, the OSM-induced suppression of adiponectin expression and dedifferentiation of adipocytes were ameliorated by WHI-P131 or U0126, but not by AG490. These results suggest that OSM inhibits adiponectin expression by inducing dedifferentiation of adipocytes through signaling pathways involving JAK3 and MEK, but not JAK2.

Adipocytes↗
PubMed2005

Exacerbation of heart failure in adiponectin-deficient mice due to impaired regulation of AMPK and glucose metabolism.

OBJECTIVE: Insulin resistance (IR) was reported to be associated with chronic heart failure (CHF). Adiponectin, an insulin-sensitizing hormone with anti-inflammatory activity, improves energy metabolism via AMP-activated protein kinase (AMPK). AMPK deficiency is associated with depressed cardiac function under stress conditions. However, it is not clear whether adiponectin plays an important role in CHF. We hypothesize that deficiency of adiponectin might result in deterioration of heart failure. METHODS: Using adiponectin null mice and their littermates, we examined the effects of adiponectin on LV pressure overload-induced cardiac hypertrophy and failure, and investigated the mechanisms involved. RESULTS: Three weeks after transverse aortic constriction (TAC), cardiac hypertrophy (evaluated from the heart-to-body weight ratio: 7.62+/-0.27 in wild-type (WT) mice, 9.97+/-1.13 in knockout (KO) mice, P<0.05) and pulmonary congestion (lung-to-body weight ratio: 9.05+/-1.49 in WT mice, 14.95+/-2.36 in KO mice, P<0.05) were significantly greater in adiponectin KO mice than WT mice. LV dimensions were also increased in KO mice. Compared with WT TAC mice, expression of AMPKalpha protein was lower, while IR was higher in KO TAC mice. CONCLUSION: These findings indicate that adiponectin deficiency leads to progressive cardiac remodeling in pressure overloaded condition mediated via lowing AMPK signaling and impaired glucose metabolism.

Adenylate Kinase↗
PubMed2006

Relationship between adiponectin, glycemic control and blood lipids in diabetic type 2 postmenopausal women with and without complication of ischemic heart disease.

BACKGROUND: Recently major adipocytokine, adiponectin, are thought to play important roles in the regulation of cardiovascular and metabolic homeostasis. We compared serum adiponectin concentrations and lipid profile in diabetic patients with and without complication of cardiovascular disease in postmenopausal women. METHODS: We included 120 female subjects between the age of 45 and 60 years. The subjects were divided into 3 groups and each group comprised of 40 subjects. First group comprised of normal healthy controls, second group diabetic type 2 patients with no history of ischemic heart disease (IHD) and the third group diabetic patients with IHD. Serum adiponectin concentrations, serum triglycerides, cholesterol, LDL cholesterol and HDL cholesterol concentrations were determined. RESULTS: Values of fasting and random blood glucose, serum triglycerides, cholesterol, LDL cholesterol were significantly increased (P<0.001) in diabetic patients with IHD as compared with normal control subjects except for serum adiponectin and HDL cholesterol concentrations, which were significantly decreased (P<0.001) in diabetic patients and diabetic patients with IHD group. When values of cholesterol, triglycerides, LDL cholesterol, HDL cholesterol, fasting and random blood glucose and adiponectin were compared among diabetic and diabetic patients with IHD, it was observed that they were significantly increased (P<0.001) except for adiponectin, which was decreased significantly (P<0.001) and random blood glucose, LDL and HDL cholesterol in which no change was observed between the 2 groups. CONCLUSIONS: Serum adiponectin concentrations may be a predictor for development of cardiovascular disease in postmenopausal diabetic patients.

Adiponectin↗
PubMed2006

Association of adiponectin and amino terminal proBNP in peripheral arterial disease.

BACKGROUND: The aim of the present study was to investigate the relationship of adiponectin, a novel adipocytokine, and amino terminal proBNP (NT-proBNP) in patients with peripheral arterial disease (PAD). METHODS: Serum concentrations of adiponectin and NT-proBNP were measured in 487 patients with symptomatic PAD from the Linz Peripheral Arterial Disease (LIPAD) study. RESULTS: Correlation analysis revealed an association of adiponectin and NT-proBNP (r, +0.47; p<0.001). Even after adjustment for age, sex, body mass index, diabetes mellitus, smoking, arterial hypertension, estimated glomerular filtration rate (eGFR), fasting glucose, LDL-cholesterol, HDL-cholesterol, triglycerides, high-sensitivity C-reactive protein, and total homocysteine the relationship of adiponectin and NT-proBNP remained significant (r, +0.35; p<0.001). Furthermore, a subgroup analysis of patients with first manifestation of symptomatic PAD (n=287) demonstrated that disease severity (classified by Fontaine stages) was positively related to adiponectin (r, +0.13; p=0.003) and NT-proBNP (r, +0.28; p<0.001). CONCLUSION: Adiponectin was positively associated with NT-proBNP in symptomatic atherosclerotic PAD, independent of traditional and non-traditional risk factors. Moreover, adiponectin and NT-proBNP were related to disease severity, indicating a possible role for assessment of future morbidity and mortality in patients with PAD.

Adiponectin↗
PubMed2006

The effect of losartan and amlodipine on serum adiponectin in Japanese adults with essential hypertension.

BACKGROUND: Adiponectin, an adipocyte-derived protein, is reduced in patients with hypertension and insulin resistance (IR). Angiotensin II receptor blockers (ARBs) have been reported to improve IR and reduce albuminuria. The purpose of this study was to evaluate the influence of an ARB and a calcium channel blocker on serum adiponectin levels in Japanese patients with hypertension who were treated with losartan or amlodipine for 3 months. METHODS: Patients with essential hypertension (EHT) were randomized to treatment prospectively with losartan (50-100 mg/d) or amlodipine (5-10 mg/d) for 3 months. Patients with renal damage and/or macroproteinuria were excluded. The urine albumin/creatinine ratio, homeostasis model assessment (HOMA) index, adiponectin concentration, and tumor necrosis factor-alpha (TNF-alpha) concentration of each patient were evaluated before and after 3 months of treatment. When the HOMA index exceeded 1.73, a patient was considered to have IR. RESULTS: All 40 participants completed both 3-month treatment periods. Study patients were primarily male (52.5%) with a mean (SD) age of 63.8 (10.6) years and a mean body weight of 60.7 (10.8) kg. Patients with EHT and diabetes mellitus (n = 9) and IR (n = 12) had significantly lower adiponectin concentrations than patients who had EHT without diabetes or IR (n = 19; mean [SD], 7.84 [5.54] vs 12.81 [7.36] microg/mL, P = 0.034; and 6.12 [3.04] vs 12.81 [7.36] microg/mL, P = 0.004, respectively). Adiponectin concentrations correlated negatively with body mass index (r = -0.393; P = 0.012) and HOMA index (r = -0.440; P = 0.005) and positively with high-density lipoprotein cholesterol (r = 0.441; P = 0.004) before treatment. Systolic blood pressure was significantly decreased in patients treated with losartan (n = 20; mean [SD], 166 [19] to 140 [15] mm Hg; P < 0.001) or amlodipine (n = 20; 164 [15] to 136 [15] mmHg; P < 0.001), and diastolic blood pressure also was significantly decreased with losartan (93 [14] to 83 [10] mm Hg; P = 0.031) or amlodipine (96 [12] to 82 [10] mm Hg; P < 0.001). Losartan increased adiponectin concentrations (9.56 [6.75] to 10.36 [6.94] microg/mL; P = 0.038), whereas amlodipine had no significant effect (9.67 [6.62] to 10.01 [6.79] microg/mL). The difference in TNF-alpha concentration before and after treatment with losartan and amlodipine did not reach statistical significance (mean [SD], 15.2 [1.4] to 14.8 [1.5] pg/mL; and 14.3 [1.4] to 14.5 [1.7] pg/mL, respectively). CONCLUSION: In this study, Japanese adults with EHT had significant increases in adiponectin after 3 months of treatment with 50 to 100 mg/d of losartan, but not with 5 to 10 mg/d of amlodipine.

Adiponectin↗
PubMed2004

Adiponectin, the missing link in insulin resistance and obesity.

Obesity and insulin resistance have been recognised as leading causes of major health issues, particularly diabetes type 2 and metabolic syndrome. Although obesity, defined as excess body fat, is frequently accompanied by insulin resistance, diabetes, metabolic syndrome and cardiovascular diseases, the molecular basis for the link between obesity and those diseases has not yet been clarified. Adipose tissue expresses various secretory proteins, including leptin, tumour necrosis factor-alpha and adiponectin, which may be involved in the regulation of energy expenditure, lipid metabolism and insulin resistance. The aim of this study is to provide an overview of the metabolic alterations occurring in insulin resistance as well as to review the biological roles of adiponectin, particularly in the regulation of fatty acid oxidation and insulin action. Adiponectin is the most abundant gene product in adipose tissue and accounts for 0.01% of total plasma protein. Plasma adiponectin level is decreased in obesity, both in children and adults, and it is negatively associated to plasma insulin and positively associated to plasma triglycerides. Low levels of adiponectin decreases fatty acid oxidation in muscle. Recent data have demonstrated that adiponectin effects are mediated by the interaction with muscle and hepatic receptors through activation of AMP kinase, the cellular "fuel gauge", which in turn inhibits acetyl CoA carboxylase and increases fatty acid beta-oxidation. Since there is no available recombinant adiponectin for human use, its direct effects on human metabolism remain unknown, but this hormone appears to be promising in the treatment of obesity an related metabolic disorders.

Adiponectin↗
PubMed2005

Adiponectin expression in human epicardial adipose tissue in vivo is lower in patients with coronary artery disease.

BACKGROUND: Intra-peritoneal adipose tissue is recognized as a predictor of metabolic syndrome and may contribute to the risk for cardiovascular disease by the production of adipocytokines, including adiponectin. Nevertheless, there is no knowledge on whether other visceral depots of adipose tissue, including the epicardial fat, have any metabolically active role, including production of adiponectin. AIM OF THE STUDY: We sought to evaluate adiponectin protein expression in epicardial adipose tissue in vivo both in patients with severe coronary artery disease (CAD) and in subjects without CAD. METHODS: Twenty-two patients were enrolled for the study. We selected 16 patients who underwent elective coronary artery bypass graft surgery for critical CAD, 5 who underwent surgery for valve replacement and 1 for correction of an interatrial defect. Epicardial adipose tissue biopsy samples were obtained before the initiation of cardiopulmonary bypass. Adiponectin protein level in epicardial adipose tissue was evaluated by Western blotting. RESULTS: Adiponectin protein value, expressed as adiponectin/actin ratio, in epicardial adipose tissue was significantly lower in patients with severe CAD than in those without CAD (1.42 +/- 0.77 vs 2.36 +/- 0.84 p = 0.02, 95% CI 0.64-1.74). CONCLUSIONS: This study showed for the first time that human epicardial adipose tissue expresses adiponectin. Adiponectin expression is significantly lower in epicardial fat isolated from patients with CAD.

Adiponectin↗
PubMed2004

Chronic treatment with growth hormone stimulates adiponectin gene expression in 3T3-L1 adipocytes.

Growth hormone (GH) is an important regulator of adiposity and systemic energy metabolism. Here, we have investigated the effects of GH on production of adiponectin, an anti-diabetic and anti-atherogenic hormone secreted exclusively from adipocytes. Analysis using real time quantitative PCR revealed that GH significantly increased adiponectin gene expression in a dose-dependent manner. Time course study showed that the expression of adiponectin gene started to increase only after 30 h of GH treatment (10(-8) M), suggesting it to be a chronic effect. GH-mediated induction of adiponectin gene expression was completely blocked by treatment with the Janus kinase2 (JAK2) inhibitor AG490 and the P38 mitogen activated protein (MAP) kinase inhibitor SB203580, while the specific inhibitors of phosphatidylinositol-3-kinase (LY294002) and p70S6 kinase (rapamycin) moderately enhanced GHs effect. Co-incubation of adipocytes with GH and the PPARgamma agonist rosiglitazone produced additive effects on induction of adiponectin gene expression. These results collectively suggest that GH increases adiponectin gene expression through the JAK2-P38 MAP kinase pathway, and that elevation of adiponectin production might represent a novel mechanism by which GH regulates systemic energy metabolism and insulin sensitivity.

3T3 Cells↗
PubMed2005

Plasma adiponectin and insulin resistance in women with polycystic ovary syndrome.

OBJECTIVE: To determine plasma adiponectin concentration in women with and without polycystic ovary syndrome (PCOS) and to assess possible correlations of adiponectin to the hormonal and metabolic parameters, including measures of insulin resistance (IR). DESIGN: Case-control study. SETTING: Tertiary-referral university hospital. PATIENT(S): One hundred eighty selected women were classified as follows: 45 obese (body mass index [BMI] >30 kg/m2) with PCOS; 45 lean (BMI <25 kg/m2) with PCOS; 45 obese (BMI >30 kg/m2) without PCOS, and 45 lean (BMI <25 kg/m2) without PCOS. INTERVENTION(S): Blood samples were collected from all women with or without PCOS between 8 and 11 am, after an overnight fast. MAIN OUTCOME MEASURE(S): Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), free T4, testosterone (T), 17-alpha-hydroxyprogesterone, Delta4-androstenedione (Delta4-A), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), sex hormone-binding globulin (SHBG), insulin, and plasma levels of adiponectin and glucose. Measures of IR included fasting serum insulin, glucose-to-insulin ratio, and homeostasis model assessment (HOMA). RESULT(S): Adiponectin concentrations were found to be significantly decreased in women with PCOS and in obese women without PCOS as compared with lean women without PCOS. Adiponectin concentrations correlated inversely with body weight, BMI, fasting plasma glucose, serum insulin, Delta4-A, DHEA, DHEAS, and HOMA but correlated positively with serum T, SHBG, FAI, and glucose-to-insulin ratio. Multiple regression analysis showed that BMI, HOMA, Delta4-A, and insulin were independent determinants of adiponectin concentrations. CONCLUSION(S): Hypoadiponectinemia is evident in obese and lean women with PCOS with variable degree of IR; and it is suggested that IR per se or other metabolic abnormalities of PCOS are involved in the regulation of adiponectin concentration in women with PCOS.

Adiponectin↗
PubMed2006

Serum concentrations of adiponectin and risk of type 2 diabetes mellitus and coronary heart disease in apparently healthy middle-aged men: results from the 18-year follow-up of a large cohort from southern Germany.

OBJECTIVES: We sought to assess the association between serum concentrations of adiponectin and long-term risk of type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD) in initially healthy middle-aged men within the same representative population in Augsburg, southern Germany. BACKGROUND: It has been postulated that high serum concentrations of adiponectin, an emerging biomarker that is linked to insulin resistance and endothelial dysfunction, may be protective against T2DM and CHD. METHODS: Serum concentrations of adiponectin were determined in apparently healthy middle-aged men, sampled from the general population in 1984/1985 and followed until 2002. During this period, 115 of 887 men had a newly diagnosed T2DM, and 126 of 937 men suffered from a CHD event. RESULTS: In a Cox model, after multivariable adjustment for cardiovascular risk factors, the hazard ratio of incident T2DM, comparing extreme tertiles of the adiponectin distribution, was 0.55 (95% confidence interval [CI], 0.35 to 0.89), and for incident CHD it was 0.62 (95% CI, 0.39 to 0.98). Further adjustment for high-density lipoprotein cholesterol (HDL-C) attenuated the association, which became formally non-significant. In joint analysis, men with low adiponectin and low HDL-C values showed a 2.63 times (95% CI, 1.66 to 4.15) increased incidence of T2DM and a 1.91 times (95% CI, 1.20 to 3.04) increased incidence of CHD after multivariable adjustment in comparison with men with high HDL-C and high adiponectin. CONCLUSIONS: For patients with low HDL-C values, additional measurement of adiponectin may be helpful to identify individuals at very high risk for T2DM and CHD.

Adiponectin↗
PubMed2005

Production of mouse adiponectin, an anti-diabetic protein, in transgenic sweet potato plants.

Adiponectin is a 30kDa protein exclusively produced and secreted from adipocytes and as a cytokine has been found to link obesity, insulin resistance, and type 2 diabetes. Production of biologically active adiponectin in large scale is desirable for pharmaceutical applications. Mouse adiponectin cDNA was used for developing transgenic sweet potato plants via Agrobacterium-mediated transformation. The presence of the transgene was verified by PCR and DNA gel blot analysis. Further investigated were five independent transgenic lines, all of which expressed high levels of adiponectin mRNA. Immuno blot analysis with a mouse adiponectin antiserum revealed that, in addition to a 29 kDa-protein which co-migrates with the adiponectin protein produced in Escherichia coli cells, a 31 kDa-protein was produced, indicative of a post-translational modification of the protein. The transgenic plants did not show obvious differences in growth rate and morphology in response to adiponectin production.

Adiponectin↗
PubMed2006

Selective increase in high molecular weight adiponectin concentration in serum of women with preeclampsia.

Total adiponectin concentrations have been shown to increase in serum of preeclamptic women. However, variance of concentrations of different isoforms has not been studied, despite the emerging notion that high, medium and low molecular weight adiponectin exert different functions. We have determined serum concentrations of each adiponectin isoform using a newly developed enzyme immunosorbent assay. High molecular weight (HMW) adiponectin concentrations were significantly higher in women with preeclampsia (n=14; median, 11.2 microg/ml; interquartile range, 9.2-15.8) compared to normal pregnant women (n=14; 6.8 microg/ml, 5.4-10.7; P=0.04). In contrast, medium molecular weight and low molecular weight adiponectin concentrations were substantially equal between the groups. The ratio of HMW adiponectin to total adiponectin was also markedly higher in preeclamptic women (52.3%, 49.5-58.7) than control women (43.0%; 39.8-48.0; P=0.004). Taken together with other reports our findings imply a physiological feedback response to minimize endothelial damage in preeclamptic women.

Adiponectin↗
PubMed2005

Gestational diabetes is associated with depressed adiponectin levels.

OBJECTIVE: Adiponectin is a 29-kd adipocyte-secreted protein that has been linked to insulin resistance in obesity and diabetes. The aim of the present study was to evaluate adiponectin levels in the insulin-resistant state of diabetes in gestation. METHODS: Term, gravid subjects with diabetes (n = 31; age, 30.0 +/- 0.9 years; weight, 98.8 +/- 4.6 kg) and healthy, term, gravid subjects (n = 27; age, 26.1 +/- 1.1 years; weight, 91.2 +/- 3.78 kg) were examined. The diabetes group consisted of 11 class A1, 11 class A2, and nine class B subjects. Plasma insulin, glucose, adiponectin, and leptin were measured on samples obtained immediately before Cesarean or vaginal delivery. Data were presented as means +/- SE, and significance is set at P < or = .05. RESULTS: We observed decreased adiponectin levels in class A2 (4.93 +/- 0.58 microg/mL; P = .013) and class B diabetics (3.33 +/- 0.56 microg/mL; P = .001) as compared to controls (8.17 +/- 0.82 microg/mL), while a nonsignificant decrease was also observed in class A1 (6.58 +/- 1.13 microg/mL; P = .213). When grouping all gravid subjects, we observed that non-Caucasian subjects (n = 42) (5.51 +/- 0.51 microg/mL; P = .003) had lower adiponectin levels than Caucasian subjects (n = 16) (8.88 +/- 1.11 microg/mL). Within the non-Caucasian group, we found significantly lower adiponectin levels in diabetic gravid subjects (class A2: 4.24 +/- 0.75 microg/mL; P = .044; and class B: 3.33 +/- 0.56 microg/mL; P = .005) compared with nondiabetic gravid subjects (7.05 +/- 0.80 microg/mL). CONCLUSION: Class A2 and B gestational diabetes are associated with suppressed levels of adiponectin, similar to that found in other insulin-resistant states (type II diabetes and obesity).

Adiponectin↗